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Bisphenol S-induced inflammation: a comparative insight on inflammatory pathway activation in zebrafish and rodent models
Bisphenol S and inflammatory pathway activation
Abstract
Background. Bisphenol S (BPS) is a widespread BPA substitute with emerging immunotoxicity; this review synthesizes zebrafish and rodent experimental evidence to clarify BPS‑induced inflammation.
Methods. Narrative synthesis of experimental studies in zebrafish and rodent models, focusing on molecular pathways, organ‑level effects, and exposure timing.
Results. Across models, BPS consistently activates an oxidative stress-mediated NF‑κB axis with increased ROS, lipid peroxidation, and upregulation of TNF‑α, IL‑1β, and IL‑6; chronic and developmental low‑to‑moderate exposures produced stronger inflammatory
phenotypes than acute high doses.
Conclusions. Convergent mechanistic and pathological findings strengthen the weight of evidence for BPS immunotoxicity and support targeted monitoring and controls; key research gaps include inflammasome activation, receptor mechanisms, sex differences, mixture effects, epigenetic regulation, and standardization.
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This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
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Copyright (c) 2026 Istituto Superiore di Sanità
How to Cite
Wan Azhan, W. N. I., Zakaria, F. N., Fuad Al’arifin , D. A., Amlie, N. Z., Kamarudin, E., Paiman, F., Risandiansyah, R., & Dasiman, R. (2026). Bisphenol S-induced inflammation: a comparative insight on inflammatory pathway activation in zebrafish and rodent models: Bisphenol S and inflammatory pathway activation . Annali dell’Istituto Superiore Di Sanità, 62(3), 267–276. https://doi.org/10.4415/ANN_26_03_09
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